Antidiabetic Drugs
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| Decribe two types of diabetes | Type 1- Usually begins in childhood , Rapid onset
Unknown cause
Type 2-Adult Onset Diabetes
Genetics, it’s in your family history, Over-weight/Obesity, Little or no exercise*, immune response
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| S/Sx of diabetes | Elevated fasting blood glucose (higher than 126 mg/dL)
Polyuria,Polydipsia,Polyphagia,
Glycosuria,Unexplained weight loss, Fatigue, Hyperglycemia
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| Criteria for diagnosis for DM | Symptoms + plasma glucose level less than or equal to 200 mg/dL
OR
Fasting plasma glucose higher than or equal to 126 mg/dL
OR
2-hour postload glucose level higher than or equal to 200 mg/dL during an oral glucose tolerance test
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| what is type 1 DM | Lack of insulin production or production of defective insulin
Pts need exogenous insulin. Will starve.
Fewer than 10% of all diabetes cases are type 1
Complications:Diabetic ketoacidosis (DKA), Hyperosmolar nonketotic syndrome
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| what is type 2 DM | Most common type: 90% of all cases
Insulin deficiency and insulin resistance, glucose does not go into cell.
Many tissues are resistant to insulin
Reduced number of insulin receptors
Insulin receptors less responsive
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| Often known as metabolic syndrome or insulin resistance syndrome or syndrome X | central obesity, high BP, high triglyderides, low HDL, insulin resistance
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| what is gestational diabetes | hyperglycemia during preg.
insulin given prevent birth defects, subsides after delivery, 30% dev. type 2 DM in 10-15 yrs
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| what are major long term complications of DM | macrovascular (atherosclerotic plaque)
coronary aa, cerebral aa, peripheral vessels
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| what are major long term complications of DM | Microvascular (capillary damage)
retinopathy, neuropathy, nephropathy
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| What indicates "prediabetes" | Fasting plasma glucose (FPG) levels higher than or equal to 110 mg/dL but less than 126 mg/dL.
Screening recommended every 3 years for all patients 45 years and older
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| Treatment for DM | Type 1-Insulin therapy
Type 2- Lifestyle changes, Oral drug therapy, Insulin when the above no longer provide glycemic control
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| how do insulins fx | substitute for endogenous hormone, restores pt ability to metabolize carbs, fats, proteins, store glucose in liver, convert glycogen to fat stores
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| What are rapid acting insulins | Most rapid onset of action (5 to 15 minutes), shorter duration
Pt must eat after injection
May be given SC or via continuous SC infusionpump (but not IV)
Insulin lispro (Humalog)
Insulin aspart (NovoLog)
Insulin glulisine (Apidra)-Newest
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| What is short acting insulin | Regular insulin (Humulin R)
Onset 30 to 60 minutes
The only insulin product that can be given by IV bolus, IV infusion, or even IM
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| what is intermediate acting insulin | Isophane insulin suspension (also called NPH) - Cloudy appearance
Slower in onset and more prolonged in duration than endogenous insulin
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| what is long acting insulin | glargine (Lantus), detemir (Levemir)
Clear, colorless solution
Referred to as basal insulin
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| Common combined insulins | Combination insulin products
NPH 70% and regular insulin 30% (Humulin 70/30, Novolin 70/30, Novolog 70/30)
NPH 50% and regular insulin 50% (Humulin 50/50)
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| How is a sliding scale insulin dose determined | SC short-acting or regular insulin to blood glucose test
hospitalized pts/TPN or enteral tube feedings
Subcutaneous insulin ordered that incr as blood glucose incr.
Disadv: delays insulin adm. til hyperglycemia occurs; lg swings in glucose control
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| when can you use oral antidiabetic drugs | type 2 w/ lifestyle modifications
ex: Biguanides: Glucophage
Sulfonylureas: 1st gen-diabinese, Tolinase
2nd g- Amaryl, glucotrol, DiaBeta, Micronase
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| More oral antidiabetic drugs | Glinides: Prandin, Starlix
Thiazolidinediones: Actos, Avandia (glitazones)
Alpha-glucosidase inhibitors: Precose, Glyset
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| what are some new antidiabetic drugs | Amylin mimetics: Symlin
Incretin mimetics: Byetta, Januvia
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| What is MOA of Biguanides | Decrease production of glucose by the liver
Decrease intestinal absorption of glucose
Increase uptake of glucose by tissues
Do not increase insulin secretion from the pancreas (does not cause hypoglycemia)
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| What is MOA of Sulfonylureas | Stimulate insulin secretion from the beta cells of the pancreas, increasing insulin levels
Beta cell function must be present
Improve sensitivity to insulin in tissues
Result in lower blood glucose levels
First-generation drugs not used as frequently
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| What is MOA of Glinides | Action similar to sulfonylureas
Increase insulin secretion from the pancreas
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| What is MOA of Thiazolidinediones | Decrease insulin resistance
“Insulin sensitizing drugs”
Increase glucose uptake and use in skeletal muscle
Inhibit glucose and triglyceride production in the liver
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| What is MOA of alpha-glucosidase inhibitors | Reversibly inhibit the enzyme alpha-glucosidase in the small intestine
Result in delayed absorption of glucose
Must be taken with meals to prevent excessive postprandial blood glucose elevations (with the “first bite” of a meal)
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| what is MOA of Amylin mimetics | Mimics the natural hormone amylin
Slows gastric emptying
Suppresses glucagon secretion, reducing hepatic glucose output
Centrally modulates appetite and satiety
Used when other drugs have not achieved adequate glucose control
Subcutaneous injection
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| what is MOA of Incretin mimetics | Mimics the incretin hormones
Enhances glucose-driven insulin secretion from beta cells of the pancreas
Only used for Type 2 diabetes
Exenatide: Injection pen device
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| Adverse effects of Metformin | Primarily affects GI tract: abdominal bloating, nausea, cramping, diarrhea, feeling of fullness, also metallic taste, red.vit. B12 levels
Lactic acidosis is rare, lethal.
No hypoglycemia
Taken with meals, discontinued if pt studies with contrast dye
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| adverse effects of sulfonylureas | Hypoglycemia, hematologic effects, nausea, epigastric fullness, heartburn, may interact w/ alcohol cause disulfiram type reaction
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| adverse effects of glinides | Headache, hypoglycemic effects, dizziness, weight gain, joint pain, upper respiratory infection or flulike symptoms
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| adverse effects of thiazolidinediones | Moderate weight gain, edema, mild anemia
Hepatic toxicity—monitor ALT levels
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| adverse effects of alpha-glucosidase inhibitors | Flatulence, diarrhea, abdominal pain
Do not cause hypoglycemia, hyperinsulinemia, or weight gain
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| what is hypoglycemia | Abnormally low blood glucose level (below 50 mg/dL)
Mild cases can be treated with diet—higher intake of protein and lower intake of carbs—to prevent a rebound postprandial hypoglycemia
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| hypoglycemia ss/sx | Early
Confusion, irritability, tremor, sweating
Later
Hypothermia, seizures
Coma and death will occur if not treated
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| glucose elevating drugs | Oral forms of concentrated glucose
Buccal tablets, semisolid gel
50% dextrose in water (D50W)
Glucagon
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| if pt is NPO and on antidiabetic drug, what should you do before procedure | contact Dr to clarify orders
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| When insulin is ordered, ensure: | Correct route, Correct type of insulin, Timing of the dose, Correct dosage
Second-checked with another nurse
Check blood glucose level, Roll vials b/n hands no shake.
ONLY use insulin syringes, calibrated in units, correct timing of dose with meals
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| When drawing up insulin which do you do first | always withdraw the regular or rapid-acting insulin first
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| Pt. education wtih insulin | self-administration of insulin injections, including timing of doses, monitoring blood glucoses, and injection site rotations
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| when giving oral antidiabetic meds when should you give | 30 minutes before meals
Alpha-glucosidase inhibitors are given with the first bite of each main meal
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| What should you give if hypoglycemia occurs | conscious- oral form of glucose:glucose tablets or gel, corn syrup, honey, fruit juice, or nondiet soft drink, eat crackers or a half sandwich
Unconscious- give D50W or glucagon, intravenously, monitor blood glucose levels
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